Abstract
Psoriasis is a chronic inflammatory skin disease. It is assumed that the plaque phenotype of psoriasis is associated with T helper (Th) 1 immune response activation, while the guttate phenotype is associated with the Th17 immune response. Previous investigations of differences in the serum levels of cytokines relative to the clinical psoriatic phenotype have yielded conflicting results. This study compared the levels of circulating inflammatory cytokines and LL-37 relative to the morphological phenotype in patients with psoriasis. Seventy-four age-matched patients with psoriasis (32 with guttate psoriasis and 42 with plaque psoriasis) and 12 healthy controls were included. A multiplex cytokine assay and enzyme-linked immunosorbent assay were used to measure levels of Th1- and Th17-derived cytokines and LL-37, respectively. Circulating levels of interferon- (IFN)-γ, interleukin- (IL)-1RA, IL-2, and IL-23, and LL-37 were significantly higher in patients with psoriasis than in healthy controls. However, the serum levels of inflammatory cytokines (IL-7, IL-22, and IL-23) and LL-37 did not differ significantly between the guttate and plaque phenotypes of psoriasis. There was a positive correlation between serum inflammatory cytokine levels and the Psoriasis Area and Severity Index score. The findings of this study suggest that the serum levels of inflammatory cytokines reflect the disease activity rather than determine the morphological phenotype.
Highlights
Psoriasis is a chronic inflammatory skin disease with characteristic histological changes, including abnormal epidermal proliferation and a cellular infiltrate composed of neutrophils and T cells [1]
Psoriasis was originally classified as a T helper (Th) 1 disease because cytokines involved in the Th1 pathway, such as interferon- (IFN-) γ, interleukin- (IL-) 2, and IL-12, are elevated in lesional skin and peripheral blood [2,3,4], and the success of classical treatments is related to the result of redirecting a Th1 response towards a Th2 response [5]
Recent studies suggest that dendritic cells (DCs) and altered expression of antimicrobial peptides play a role in the pathogenesis of psoriasis
Summary
Psoriasis is a chronic inflammatory skin disease with characteristic histological changes, including abnormal epidermal proliferation and a cellular infiltrate composed of neutrophils and T cells [1]. Plasmacytoid DCs are activated through a cathelicidin LL-37 and DNA complex in a tolllike-receptor-dependent manner [8] This activation induces increased production of type I IFN, leading to myeloid DC activation and leading to Th1/Th17 differentiation and keratinocyte activation [9]. This subsequently induces the expression of various cytokines [10, 11]. The present study compared differences in the serum levels of circulating Th1 and Th17 cytokines between plaque and guttate psoriasis and investigated the correlation between disease activity and serum levels of inflammatory cytokines. Serum LL-37 levels in patients with psoriasis were compared with those in healthy controls, and the correlations between serum levels of LL-37 and inflammatory cytokines were analyzed
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